Specter S E, Hamilton J S, Stern J S, Horwitz B A
Department of Nutrition, School of Medicine, University of California, Davis 95616, USA.
J Nutr. 1995 Aug;125(8):2183-93. doi: 10.1093/jn/125.8.2183.
Attenuated regulatory thermogenesis in genetically obese (fa/fa) Zucker rats involves an impaired capacity to increase sympathetic drive to brown adipose tissue in response to dietary stimuli. Young, growing lean rats fed a low protein diet reduce energetic efficiency to compensate for elevated energy intake; however, it is not known if obese rats adapt similarly to chronic protein restriction by decreasing energetic efficiency and whether this would be accompanied by increased brown adipose tissue thermogenic capacity. Lean (Fa/Fa) and obese Zucker rats were either protein-restricted (protein 8% of total energy) or fed a control diet (21% protein) starting at age 5 wk. At 9 wk, oxygen consumption (VO2) was measured in response to an intubated meal of mixed macronutrient composition. Mass-adjusted food intake (i.e., food intake/body weight 0.67) was greater in protein-restricted than in control lean rats, but not different due to diet in obese rats. Mass-adjusted brown adipose tissue uncoupling protein levels were more than 100% greater in protein-restricted vs. control lean rats, but not different between protein-restricted and control obese rats. The uncoupling protein level was not significantly different in control lean vs. obese rats. Energetic efficiency was 40% lower in protein-restricted vs. control lean, but not different in obese rats; however, the efficiency of protein utilization was significantly greater in obese protein-restricted than in obese control rats. Meal-induced energy expenditure (VO2) did not differ significantly due to diet or genotype. In conclusion, protein restriction led to overfeeding in lean rats which appeared to enhance brown adipose tissue thermogenic capacity and decrease energetic efficiency. Protein efficiency increased to more than two times its original value in obese (fa/fa) rats, but otherwise no metabolic accommodation in the capacity for regulatory thermogenesis was observed in this genotype.
遗传性肥胖（fa/fa） Zucker大鼠的适应性产热减弱，这涉及到其在饮食刺激下增加对棕色脂肪组织交感神经驱动的能力受损。给幼年生长中的瘦大鼠喂食低蛋白饮食会降低能量效率，以补偿能量摄入的增加；然而，尚不清楚肥胖大鼠是否会通过降低能量效率来类似地适应慢性蛋白质限制，以及这是否会伴随着棕色脂肪组织产热能力的增加。从5周龄开始，将瘦（Fa/Fa） Zucker大鼠和肥胖Zucker大鼠分别进行蛋白质限制（蛋白质占总能量的8%）或喂食对照饮食（21%蛋白质）。在9周龄时，通过插管喂食混合宏量营养素组成的食物，测量氧气消耗量（VO2）。蛋白质限制组的瘦大鼠经体重调整后的食物摄入量（即食物摄入量/体重0.67）高于对照瘦大鼠，但肥胖大鼠的饮食组间无差异。蛋白质限制组的瘦大鼠经体重调整后的棕色脂肪组织解偶联蛋白水平比对照瘦大鼠高100%以上，但蛋白质限制组和对照肥胖大鼠之间无差异。对照瘦大鼠和肥胖大鼠的解偶联蛋白水平无显著差异。蛋白质限制组的瘦大鼠能量效率比对照瘦大鼠低40%，但肥胖大鼠无差异；然而，肥胖蛋白质限制组大鼠的蛋白质利用效率显著高于肥胖对照组大鼠。饮食或基因型对进食诱导的能量消耗（VO2）无显著差异。总之，蛋白质限制导致瘦大鼠过度进食，这似乎增强了棕色脂肪组织的产热能力并降低了能量效率。肥胖（fa/fa）大鼠的蛋白质效率增加到其原始值的两倍以上，但在该基因型中未观察到调节性产热能力的其他代谢适应性变化。
